Levenson Cathy W
Florida State University, Program in Neuroscience, Department of Nutrition, Food & Exercise Sciences, 237 Biomedical Research Facility, Tallahassee, FL 32306-4340, USA.
Nutr Rev. 2003 Jul;61(7):247-9. doi: 10.1301/nr.2003.jul.247-249.
The role of neuropeptide Y (NPY) in feeding behavior and zinc deficiency-induced anorexia has been controversial because hypothalamic NPY levels are elevated in both zinc deficiency and food restriction. A recent report shows that while NPY is released from terminals in the paraventricular nucleus of the hypothalamus of food-restricted animals, this release is significantly impaired in zinc-deficient animals. Zinc deficiency may therefore cause anorexia by inhibiting the release of NPY that is required for receptor activation.
神经肽Y(NPY)在进食行为和锌缺乏所致厌食症中的作用一直存在争议,因为在锌缺乏和食物限制状态下,下丘脑NPY水平均会升高。最近一份报告显示,虽然在食物受限动物的下丘脑室旁核中,NPY从终末释放,但在缺锌动物中这种释放明显受损。因此,锌缺乏可能通过抑制受体激活所需的NPY释放而导致厌食。